When LNCaP and 22Rv1 cells, two prostate cancer cell lines carrying the wild-type copy of the TP53 gene, were treated with the dual inhibitor RO, or with a combination of nutlin-3 and SJ, p53 was stabilized and activated, since both treatments disrupted the p53 interaction with MDM2 and MDMX. This evidence concerns the gene TP53 and prostate cancer.